β-adrenergic or parasympathetic inhibition, heart rate and cardiac output during normoxic and acute hypoxic exercise in humans

Acute hypoxia increases heart rate (HR) and cardiac output (V-O2) at a given oxygen consumption (V-O2) during submaximal exercise. It is widely believed that the underlying mechanism involves increased sympathetic activation and circulating catecholamines acting on cardiac receptors. Recent evidence indicating a continued role for parasympathetic modulation of HR during moderate exercise suggests that increased parasympathetic withdrawal plays a part in the increase in HR and 0, during hypoxic exercise. To test this, we separately blocked the 8-sympathetic and parasympathetic arms of the autonomic nervous system (ANS) in six healthy subjects (five male, one female; mean S.E.M. age = 31.7 +/- 1.6 years, normoxic maximal V-O2 (V-O2,(max)) = 3.1 +/- 0.31 min(-1) during exercise in conditions of normoxia and acute hypoxia (inspired oxygen fraction = 0.125) to VO2,(max). Data were collected on different days under the following conditions: (I)control, (2) after 8.0 mg propranolol i.v. and (3) after 0.8 mg glycopyrrolate i.v. O-t was measured using open-circuit acetylene uptake. Hypoxia increased venous [adrenaline] and [noradrenaline] but not (dopamine] at a given V-O2, (P < 0.05, P < 0.01 and P = 0.2, respectively). HR/V-O2 and Q(t)/V-O2 increased during hypoxia in all three conditions (P < 0.05). Unexpectedly, the effects of hypoxia on HR and Q(t), were not significantly different from control with either beta-sympathetic or parasympathetic inhibition. These data suggest that although acute exposure to hypoxia increases circulating [catecholamines], the effects of hypoxia on HR and Q(t) do not necessarily require intact cardiac muscarinic and receptors. It may be that cardiac a receptors play a primary role in elevating HR and Q(t) during hypoxic exercise, or perhaps offer an alternative mechanism when other ANS pathways are blocked.